Whether AT3 will turn out to be of benefit in Stroke (thrombotic and certainly not hemorrhagic) and heart attack only time will tell. In the mean time its fun to discuss this realising we have only ideas and opinions. I would like to take the other side. I see a very good chance AT3 will be of benefit to both conditions and cite both the thrombin study Dew mentioned as well as the re-perfusion paper. My guess is if there were systemic problems the drug could be administered locally via angio placed catheter. Hemorrhagic conditions would no doubt represent some form of relative or absolute contraindication. Many of the elements of the coagulation cascade are serine proteases. The body uses cascade systems when it wants to localize an effect, eg. blood clotting, to one area but not let it spread to areas where the effect would be harmful. The body likes to use serine proteases in its cascades. It makes sense to me the event triggered cell death in areas surrounding the ischemia in both thrombotic CVAs and AMIs would be a cascade system. Liu's paper which showed a serine protease inhibitor 2A inhibited capase independent cell death in PCD gives added hope for AT3.
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